Vasopressin-induced pulmonary vasodilation in rats.
Vasopressin-induced pulmonary vasodilation in rats.
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加压素诱导大鼠肺血管舒张。
DOI：
10.1152/ajpheart.1989.257.2.h415
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Voelkel,NF
中科院分区：
文献类型：
--
作者：
Walker,BR;HaynesJr,J;Wang,HL;Voelkel,NF
通过实验观察大鼠肺血管对外源性和内源性精氨酸加压素（AVP）的反应。采用体外和体内两种方法来研究AVP的直接肺血管活性特性以及这些特性如何影响完整动物的肺血流动力学。在清醒、不受约束的大鼠中，持续输注AVP （4.0 μ k -1）。min-1 iv)导致平均肺动脉压（PAP）下降，尽管全身压升高。与PAP下降相一致的是心输出量和心率的类似减少。同样，AVP的大剂量给药也能降低PAP，并且这种作用在缺氧时增强。另一系列实验考察了动脉低氧血症释放的内源性AVP对清醒大鼠肺血流动力学的影响。特定的v1抗利尿激素拮抗剂对PAP对缺氧的反应没有影响；然而，在v1拮抗剂作用后，全身耐药性趋于下降。为了确定AVP独立于这些血流变化的血管活性特性，在离体灌注的大鼠肺上进行了一系列实验。向离体肺循环注射25,200或2,000 mU AVP在常氧条件下没有效果。相反，在持续的缺氧肺血管收缩期间注射25mu AVP可引起可复制的肺血管扩张。这种血管扩张反应不受甲氯芬酯或血小板活化因子受体拮抗剂SRI 63-441的影响，但被一种特异性的v1血管加压能拮抗剂阻断。我们得出结论，尽管AVP具有深刻的全身血管收缩作用，但体内肺循环似乎相对不受外源性或内源性AVP的影响。（摘要删节250字）
Experiments were performed to determine the pulmonary vascular responses to exogenous or endogenous arginine vasopressin (AVP) in rats. Both in vitro and in vivo approaches were used to examine the direct pulmonary vasoactive properties of AVP and how those properties affect pulmonary hemodynamics in the intact animal. In conscious, unrestrained rats, constant infusion of AVP (4.0 mU.kg-1.min-1 iv) resulted in a fall in mean pulmonary artery pressure (PAP), although systemic pressure was increased. Coincident with the fall in PAP were similar reductions in cardiac output and heart rate. Similarly, bolus administration of AVP reduced PAP, and this effect was augmented during hypoxia. Another series of experiments examined the effect of endogenous AVP released by arterial hypoxemia on pulmonary hemodynamics in conscious rats. Administration of a specific V1-vasopressinergic antagonist had no effect on the PAP response to hypoxia; however, systemic resistance tended to fall following V1-antagonism. To determine the vasoactive properties of AVP independent of these changes in blood flow, a series of experiments were performed on isolated, perfused rat lungs. Injection of 25, 200, or 2,000 mU of AVP into the circulation of the isolated lung was without effect under normoxic conditions. In contrast, 25 mU AVP elicited reproducible pulmonary vasodilation when injected during ongoing hypoxic pulmonary vasoconstriction. This vasodilatory response was unaffected by meclofenamate or by the platelet-activating factor receptor antagonist SRI 63-441, but was blocked by a specific V1-vasopressinergic antagonist. We conclude that although AVP exerts profound systemic vasoconstriction, the pulmonary circulation appears relatively unaffected by exogenous or endogenous AVP in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)